Attention As Of

We are currently seeking potential graduate students with an interest in pursuing either MSc or PhD degrees. Postdoctoral researchers that have experience working with mouse models of cancer are also welcome. Apply by email to Dr. David Dankort ( with the subject line “Graduate Studies Application” and a copy of your most up to date CV.

Quick Overview

Cancer represents a failure of built-in protection mechanisms to quell rogue cells that have sustained oncogenic mutations. RAS and BRAF are the two most prevalent mutated oncogenes found in human cancers, particularly in lung cancer (~30%) and melanoma (~85%) where they function in the Ras-activated Raf-Mek-Erk kinase pathway. Additionally, there is a constellation of tumour suppressor loss in these cancers; particularly losses in p53, PTEN, and INK4a/ARF. Despite the enumeration of genetic lesions from human cancer data, there remains a lack of understanding of how these oncogenes and tumour suppressors contribute to the evolution of malignancy. For instance, aberrant activation of the Ras-activated Raf-Mek-Erk pathway can paradoxically induce a sustained cell cycle arrest, suggesting additional genes cooperate to permit tumour formation and/or progression. Armed with the vast array of genetic and molecular tools afforded to those who work with the mouse as a model organism, our lab seeks to: (1) Define these cooperating genes and how they function (2) Establish when they are important in the evolution of a tumour and (3) Determine the proper cell to target for destruction within a tumor.